Background

Aortic dissection is defined as separation of the layers within the aortic wall. Tears in the intimal layer result in the propagation of dissection (proximally or distally) secondary to blood entering the intima-media space.

This disease was first described long ago (>200 y), but new challenges have arisen since the advent of advanced diagnostic and therapeutic modalities. The clinical manifestations are diverse, making the diagnosis difficult and requiring a high clinical index of suspicion.[1, 2, 3]

Aortic dissection can be diagnosed premortem or postmortem because many patients die before presentation to the emergency department (ED) or before diagnosis is made in the ED.

Aortic dissection is more common in males than in females, with a male-to-female ratio of 2:1. The condition commonly occurs in persons in the sixth and seventh decades of life.[3] Patients with Marfan syndrome present earlier, usually in the third and fourth decades of life.

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Aortic dissection. CT scan showing a flap (right side of image).

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Aortic dissection. CT scan showing a flap (center of image).

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Aortic dissection. CT scan showing a flap (center of image).

For more examples of aortic dissection visible on CT scans, see the Multimedia section.

History of the Procedure

Morgagni first described aortic dissection more than 200 years ago. The condition was associated with a high mortality rate before the introduction of the cardiopulmonary bypass in the 1950s, which led to aortic arch repair and construction.

Recent advancements in the field of stent placements and percutaneous aortic fenestrations have further reduced mortality rates. However, despite recent advancements, the mortality rate associated with aortic dissection remains high.[1, 3]

Problem

An aortic dissection is a split or partition in the media of the aorta; this split is frequently horizontal or diagonal. An intimal tear connects the media with the aortic lumen, and an exit tear creates a true lumen and a false lumen. The true lumen is lined by intima, and the false lumen is within the media.

Typically, flow in the false lumen is slower than in the true lumen, and the false lumen often becomes aneurysmal when subjected to systemic pressure. The dissection usually stops at an aortic branch vessel or at the level of an atherosclerotic plaque.

An acute aortic dissection (< 2 wk) is associated with high morbidity and mortality rates (highest mortality in the first 7 d) compared with chronic aortic dissection (>2 wk), which has a better prognosis.

Epidemiology

Frequency

In the United States, aortic dissection is an uncommon disease. The true prevalence of aortic dissection is difficult to estimate, and most estimates are based on autopsy studies. Evidence of aortic dissection is found in 1-3% of all autopsies (1 in 350 cadavers). The incidence of aortic dissection is estimated to be 5-30 cases per 1 million people per year. Aortic dissection occurs once per 10,000 patients admitted to the hospital; approximately 2,000 new cases are reported each year in the United States.[4]

Pathophysiology

The aortic wall is continuous and is exposed to high pulsatile pressure and shear stress (the steep slope of the pressure curve, ie, the water hammer effect), making the aorta particularly prone to injury and disease from mechanical trauma. The aorta is more prone to rupture than any other vessel, especially with the development of aneurysmal dilatation, because its wall tension, as governed by the Laplace law (proportional to the product of pressure and radius), is intrinsically high.

An intimal tear connects the media with the aortic lumen, and an exit tear creates a true lumen and a false lumen. The true lumen is lined by intima, and the false lumen is lined by media. The true lumen is frequently smaller than the false lumen, but not invariably. The false lumen is indeed within the media, but suggesting that it is "lined" with it is misleading; if the aortic dissection becomes chronic, the lining becomes a serosal pseudointima. Typically, flow in the false lumen is slower than flow in the true lumen, and the false lumen often becomes aneurysmal when subjected to systemic pressure.

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Aortic dissection. True lumen versus false lumen in an intimal flap.

The dissection usually stops at an aortic branch vessel or at the level of an atherosclerotic plaque. Most classic aortic dissections begin at 1 of 3 distinct anatomic locations, including (1) the aortic arch, (2) approximately 2.2 cm above the aortic root, or (3) distal to the left subclavian artery.

Ascending aortic involvement may result in death from wall rupture, hemopericardium and tamponade, occlusion of the coronary ostia with myocardial infarction, or severe aortic insufficiency. The nervi vascularis (ie, bundles of nerve fibers found in the aortic adventitia) are involved in the production of pain.

Image A represents a Stanford A or a DeBakey type 1 dissection. Image B represents a Stanford A or DeBakey type II dissection. Image C represents a St....

Presentation

Patients with acute aortic dissection present with the sudden onset of severe and tearing chest pain, although this description is not universal. Some patients present with only mild pain, often mistaken for a symptom of musculoskeletal conditions located in the thorax, groin, or back. Some patients present with no pain.[6]

Consider thoracic aortic dissection in the differential diagnosis of all patients presenting with chest pain. The pain is usually localized to the front or back of the chest, often the interscapular region, and typically migrates with propagation of the dissection.

The pain of aortic dissection is typically distinguished from the pain of acute myocardial infarction by its abrupt onset, although the presentations of the two conditions overlap to some degree and are easily confused. Aortic dissection can be presumed in patients with symptoms and signs suggestive of myocardial infarction but without classic ECG findings.

Presenting signs and symptoms in acute thoracic aortic dissection include the following:

Anterior chest pain is a manifestation of ascending aortic dissection. Neck or jaw pain is a manifestation of aortic arch dissection. Interscapular tearing or ripping pain is a manifestation of descending aortic dissection.

Neurologic deficits are a presenting sign in up to 20% of cases. Syncope is part of the early course of aortic dissection in approximately 5% of patients and may be the result of increased vagal tone, hypovolemia, or dysrhythmia.[6] Cerebrovascular accident (CVA) symptoms include hemianesthesia and hemiparesis or hemiplegia.[6] Altered mental status is also reported. Other causes of syncope or altered mental status include (1) CVA from compromised blood flow to the brain or spinal cord or (2) ischemia from interruption of blood flow to the spinal arteries.

Patients with peripheral nerve ischemia can present with numbness and tingling in the extremities, limb paresthesias, pain, or weakness.

Horner syndrome is caused by interruption in the cervical sympathetic ganglia and manifests as ptosis, miosis, and anhidrosis.

Hoarseness from recurrent laryngeal nerve compression has also been described.

Cardiovascular manifestations involve symptoms and signs suggestive of congestive heart failure[6] secondary to acute severe aortic regurgitation or dyspnea, orthopnea, bibasilar crackles, or elevated jugular venous pressure. Signs of aortic regurgitation include bounding pulses, wide pulse pressure, and diastolic murmurs. Hypertension may result from a catecholamine surge or underlying essential hypertension.[7, 6] Hypotension is an ominous finding and may be the result of excessive vagal tone, cardiac tamponade, or hypovolemia from rupture of the dissection.

Other cardiovascular manifestations include findings suggestive of cardiac tamponade (eg, muffled heart sounds, hypotension, pulsus paradoxus, jugular venous distension); these may be present and must be recognized quickly. Superior vena cava syndrome can result from compression of the superior vena cava from a large, distorted aorta. Wide pulse pressure and pulse deficit or asymmetry of peripheral pulses is reported. Patients with right coronary artery ostial dissection may present with acute myocardial infarction, commonly inferior myocardial infarction. Pericardial friction rub may occur secondary to pericarditis.

Respiratory symptoms can include dyspnea and hemoptysis if dissection ruptures into the pleura or if tracheal or bronchial obstruction has occurred. Physical findings of a hemothorax may be found if the dissection ruptures into the pleura.

GI symptoms include dysphagia, flank pain, and/or abdominal pain. Dysphagia may occur from compression of the esophagus. Flank pain may be present if the renal artery is involved. Abdominal pain may be present if the dissection involves the abdominal aorta.

Other nonspecific clinical presentations include fever or anxiety and premonitions of death.[8]

Relevant Anatomy

From outside to inside, the aorta is composed of the intima, media, and adventitia. The intima, the innermost layer, is thin, delicate, lined by endothelium, and easily traumatized.

The media is responsible for imparting strength to the aorta and is composed of laminated but intertwining sheets of elastic tissue. The arrangement of these sheets in a spiral provides the aorta with its maximum allowable tensile strength. The aortic media contains very little smooth muscle and collagen between the elastic layers and thus has increased distensibility, elasticity, and tensile strength. This contrasts with peripheral arteries, which, in comparison, have more smooth muscle and collagen between the elastic layers.

The outermost layer of the aorta is adventitia. This largely consists of collagen. The vasa vasorum, which supplies blood to the outer half of the aortic wall, lies within the adventitia. The aorta does not have a serosal layer.

The aorta plays an integral role in the forward circulation of the blood in diastole. During left ventricular contraction, the aorta is distended by blood flowing from the left ventricle, and kinetic energy from the ventricle is transformed into potential energy stored in the aortic wall. During recoil of the aortic wall, this potential energy is converted to kinetic energy, propelling aortic lumen blood into the periphery.

The volume of blood ejected into the aorta, the compliance of the aorta, and resistance to blood flow are responsible for the systolic pressures within the aorta. Resistance is mainly due to the tone of the peripheral vessels, although the inertia exerted by the column of blood during ventricular systole also plays a small part.

The aorta has thoracic and abdominal regions. The thoracic aorta is divided into the ascending, arch, and descending segments; the abdominal aorta is divided into suprarenal and infrarenal segments.

The ascending aorta is the anterior tubular portion of the thoracic aorta from the aortic root proximally to the innominate artery distally. The ascending aorta is 5 cm long and is made up of the aortic root and an upper tubular segment. The aortic root consists of the aortic valve, sinuses of Valsalva, and left and right coronary arteries. The aortic root extends from the aortic valve to the sinotubular junction. The aortic root supports the base of the aortic leaflets and allows the 3 sinuses of Valsalva to bulge outward, facilitating the full excursion of the leaflets in systole. The left and right coronary arteries arise from these sinuses.

The upper tubular segment of the ascending aorta starts at the sinotubular junction and ends at the beginning of the aortic arch. The ascending aorta lies slightly to the right of the midline, with its proximal portion in the pericardial cavity. Structures around the aorta include the pulmonary artery anteriorly; the left atrium, right pulmonary artery, and right mainstem bronchus posteriorly; and the right atrium and superior vena cava to the right.

The arch of the aorta curves upward between the ascending and descending aorta. The brachiocephalic arteries originate from the aortic arch. Arteries that arise from the aortic arch carry blood to the brain via the left common carotid, innominate, and left subclavian arteries. Initially, the aortic arch lies slightly left and in front of the trachea and ends posteriorly to the left of the trachea and esophagus. Inferior to the arch is the pulmonary artery bifurcation, the right pulmonary artery, and the left lung. The recurrent laryngeal nerve passes beneath the distal arch, and the phrenic and vagus nerves lie to the left. The junction between the aortic arch and the descending aorta is called the aortic isthmus. The isthmus is a common site for coarctations and trauma.

The descending aorta extends from distal to the left subclavian artery to the 12th intercostal space. Initially, the descending aorta lies in the posterior mediastinum to the left of the course of the vertebral column. It passes in front of the vertebral column in its descent and ends behind the esophagus before passing through the diaphragm at the level of the 12th thoracic vertebra. The abdominal aorta extends from the descending aorta at the level of the 12th thoracic vertebra to the level of bifurcation at the fourth lumbar vertebra. The splanchnic arteries branch from the abdominal aorta. The thoracoabdominal aorta is the combination of the descending thoracic and abdominal aorta.

With increasing age, the elasticity and distensibility of the aorta decline, thus inducing the increase in pulse pressure observed in elderly individuals. The progression of this process is exacerbated in patients with hypertension, coronary artery disease, or hypercholesterolemia. The loss of physiologic distensibility is observed anatomically by fragmentation of elastin and the resultant increase in collagen. This results in an increased collagen-to-elastin ratio. This, along with impairment in flow in the vasa vasorum, may be responsible for the age-related changes. These factors cumulatively lead to increased left ventricular systolic pressure and wall tension with associated increases in end-diastolic pressure and volume.

Laboratory Studies

Aortic dissection is usually diagnosed using imaging techniques before the result of blood work is interpreted.

Leukocytosis may be present, which usually represents a stress state.

BUN and creatinine levels are elevated, possibly indicating involvement of the renal arteries or prerenal azotemia resulting from blood loss or associated dehydration (mainly when the BUN-to-creatinine ratio is >20).

Myocardial muscle creatine kinase isoenzyme, myoglobin, and troponin I and T levels are elevated if the dissection has involved the coronary arteries and caused myocardial ischemia.

Acute anemic states with a decrease in hemoglobin and hematocrit values are ominous findings suggesting that the dissection is leaking or has ruptured.

Hematuria, oliguria, and even anuria (< 50 mL/d) may occur if the dissection involves the renal arteries.

Smooth muscle myosin heavy-chain assay is performed in the first 24 hours.

Increased levels in the first 24 hours are 90% sensitive and 97% specific.

Levels are highest in the first 3 hours.

Cutoff of 2.5 has sensitivity, specificity, and accuracy of 91%, 98%, and 96% compared with normal and 88% compared with acute myocardial infarction.

This assay has greater sensitivity and specificity than transthoracic echocardiography (TTE), CT scanning, and aortography but less sensitivity and specificity than transesophageal echocardiography (TEE), MRI, and helical CT scanning.

The lactate dehydrogenase level is elevated because of hemolysis in the false lumen.

Imaging Studies

Aortic dissection can be diagnosed with imaging techniques based on whether or not the patient is hemodynamically stable.

Chest radiography is the initial imaging technique and may or may not reveal any abnormality.

An absence of mediastinal widening is observed in 40% of patients. With type A, an abnormal aortic contour is observed in a minority of patients. An absence of both is observed in 20% of patients.

Other chest radiograph findings include deviation of the trachea to the right or pleural effusion. No abnormality is observed in 12% of patients.

CT scanning with contrast is used more frequently in ED settings.

CT scanning is useful only in hemodynamically stable patients because of its lack of portability and its potential limitations in patients with contraindications to intravenous contrast agents.

Emergency CT angiography with 3-dimensional reconstruction is rapidly becoming the diagnostic test of choice. It provides detailed anatomical definition of the dissection as well as information on plaque formation. Limited availability of 3-D reconstruction in smaller centers may be a limiting factor in the use of this diagnostic modality.[9]

Pleural effusion can be seen on CT scan.

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Aortic dissection. Left subsegmental atelectasis and left plural effusion. Flap at lower right of image.

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Aortic dissection. Significant left plural effusion.

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Aortic dissection. Intimal flap and left plural effusion.

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Aortic dissection.

Echocardiography is an important imaging modality for detecting aortic dissection.[10, 11]

TEE is preferable to TTE.[11] TEE is as accurate as CT scanning and MRI in terms of sensitivity and specificity.

TEE has more advantages than other imaging techniques because it is portable and can be used in hemodynamically unstable patients; however, obesity, a narrow intercostal space, pulmonary emphysema, and mechanical ventilation decrease the accuracy of TEE.

In one study, detection of intimal flaps occurred in 100% of type A patients (in 18 of 18 with type A using biplanar views, in 10 of 39 with type B using biplanar views). Intimal tears were detected in 15 (83%) patients with type A and in 35 (90%) patients with type B (both confirmed by surgery or angiography). Intimal entry was detected in 16 of 18 patients using biplanar views and in 34 of 39 patients using single planar views. Using longitudinal views, only 2 intimal entries were detected in 18 patients. Using biplanar views, the intimal entries in 2 patients with type B entries were not visualized by TEE because the dissection was in the aortic arch and was obscured by the trachea and the left main stem bronchus. The intimal entries in 2 patients with type B entries were in the abdominal aorta.

Color Doppler TEE using biplanar views has the advantages of additional acoustic windows, ease of spatial orientation, more accurate visualization of the entry, and ease of application.

False positive results with TEE ranges about 10%[10, 11]

MRI is as accurate as CT scanning in the diagnosis of aortic dissection. Its use is limited because it is not portable.[12]

MRI may benefit patients who have adverse reactions to the use of intravenous contrast agents; the use of MRI with gadolinium is an alternative.

MRI and TEE have 100% sensitivity, and TTE has 82% sensitivity. MRI has 100% specificity and TEE has 68% specificity.

In patients with type A, MRI is 100% sensitive and specific while TEE is 100% sensitive and 78% specific. In patients with type B, MRI is 100% sensitive and specific, while TEE is 90% sensitive and 97% specific. With regard to epiphenomena, visualization of the site and spatial extent of the intimal flap with TEE is 78%, 94%, and 92% specific in the ascending, arch, and descending aorta, respectively. MRI and TEE are equal in the detection of the site of entry of the aortic dissection. TEE is 75% sensitive and MRI is 100% sensitive in the detection and localization of intraluminal thrombi.[13]

Other Tests

Diagnostic Procedures

Aortography is the criterion standard but is difficult to perform in patients with hemorrhage, shock, and/or cardiac tamponade. Aortography is not performed frequently in current practice because of risks associated with invasiveness and adverse reactions to intravenous contrast agents.

Medical Therapy

Initiate medical therapy as soon as the diagnosis is considered. The goal is to decrease the blood pressure and the shearing forces of myocardial contractility in order to decrease the intimal tear and propagation of the dissection.

Admit the patient to the intensive care unit or coronary care unit for hemodynamic studies, as follows:

Initiate therapy to reduce cardiac contractility. Administer drugs with negative inotropic effects, such as beta-blockers (the agents of choice); administer calcium channel blockers if beta-blockers are contraindicated. The following beta-blockers are commonly used:

Intravenous or oral labetalol

Intravenous or oral propranolol

Intravenous or oral esmolol

Initiate therapy to reduce systemic arterial pressure and shear stress if the patient's blood pressure allows for this type of intervention. The following agents are commonly used:

Pain management is always difficult in persons with aortic dissection. Narcotics and opiates are the preferred agents. Medical therapy is also administered to surgical patients preoperatively, intraoperatively, and postoperatively to prevent progression or recurrence of aortic dissection.

Surgical Therapy

The major objectives of surgery for aortic dissection are to alleviate the symptoms, decrease the frequency of complications, and prevent aortic rupture and death.

Improved cardiopulmonary bypass circuits have decreased the prevalence of injury to blood elements. A decrease in complications such as brain injury has resulted from a more detailed understanding of the physiology and limitations of hypothermic circulatory arrest.

Aortic arch repair and reconstruction can be partial or complete. A number of advances have resulted in a decreased frequency of complications associated with surgery on the aorta. Dacron grafts with impregnated collagen or gelatin have been developed that are impervious to blood.

Adjunct procedures, including distal aortic perfusion, profound hypothermia, cerebrospinal fluid drainage, and monitoring of somatosensory and motor evoked potentials in the brain and spinal cord, have decreased the frequency of procedure-related spinal cord injury during descending aorta and thoracoabdominal surgeries.

Percutaneous fenestrations and stent placements are performed. The area of the aorta with the intimal tear is usually resected and replaced with a Dacron graft.

The operative mortality rate is usually less than 10%; serious complications are rare with ascending aortic dissections.

Morbidity and mortality rates associated with this highly invasive surgery have decreased with the introduction of profound hypothermic circulatory arrest and retrograde cerebral perfusion.[14]

Dissections involving the arch are more complicated than those involving only the ascending aorta because the innominate, carotid, and subclavian vessels branch from the arch. Deep hypothermic arrest is usually required. If the arrest time is less than 45 minutes, the rate of CNS complications is less than 10%. Retrograde cerebral perfusion may improve the protection of the CNS during the arrest period.

The mortality rate associated with aortic arch dissections is approximately 10-15%, with significant neurologic complications occurring in an additional 10% of patients.

Medical management remains the treatment of choice for descending aortic dissections unless they are leaking or ruptured. With the progress in stenting technology, descending dissections can be approached with this modality in selected cases.[15, 16, 17, 18, 3, 5]

Preoperative Details

Numerous factors may increase mortality and morbidity rates for surgical intervention on the aorta, including a history of myocardial infarction, respiratory failure, renal failure, or stroke.

Preoperative evaluation is, therefore, essential in patients with these histories. Because aortic dissection is more common in elderly patients (ie, aged 70-80 y), this group of patients has different comorbidities.

Patients older than 50 years have a high prevalence of atherosclerotic heart disease and may require a thorough cardiac workup. Symptoms of aortic dissection are always difficult to differentiate from those of myocardial infarction.

Patients with valvular heart disease undergo workups with echocardiography or coronary angiography. If any valvular abnormalities are found, then appropriate surgical correction (valve replacement or commissurotomy) is performed prior to or simultaneous with aortic repair.

Surgeries involving the descending or thoracoabdominal aorta require a lateral thoracotomy. A history of smoking or chronic obstructive pulmonary disease is of significant concern; perform pulmonary function testing on such patients. Additionally, arterial blood gas testing may be required. In elective cases, treat reversible restrictive diseases and excessive sputum production with antibiotics and bronchodilators.

Preoperative renal dysfunction is considered the most important predictor of postoperative acute renal failure (ARF). Preoperative management involves adequate hydration and avoidance of hypotension, a low cardiac output state, and hypovolemia in order to decrease the frequency of ARF.

Perform appropriate workups for patients presenting with any neurological signs suggestive of CNS pathology (eg, stroke). This usually consists of Doppler imaging of the carotid arteries and, if needed, angiography of brachiocephalic and intracranial arteries. If the study findings are positive, perform a carotid endarterectomy before the aortic surgery.

Intraoperative Details

The objectives of surgical therapy for aortic dissection are to resect the damaged segment, excise the intimal tear, and obliterate the entry into in the false lumen. Suturing the edges of the dissected aorta both proximally and distally obliterates the entry into the false lumen. The desirability of obliterating the entrance to the false lumen is controversial because of multiple portals. Aortic continuity after dissection of a diseased segment is reestablished by means of a prosthetic sleeve graft between the 2 ends of the aorta.

Patients with type A dissections are treated with immediate surgical correction. This involves transfer to the operating room, where median sternotomy is performed. Profound hypothermia is initiated after the patient is placed on cardiopulmonary bypass. Cardiopulmonary bypass is performed by femoral-femoral cannulation and through the superior vena cava for retrograde cerebral perfusion. Myocardial temperature is kept below 15°C (59°F) by cardioplegic perfusion via the coronary sinus. This provides myocardial protection throughout the procedure. Ventricular distension is avoided by decompressing the left ventricle by venting through the left superior pulmonary vein or artery. The pump is stopped when the electroencephalogram is isoelectric and the nasopharyngeal temperature reaches 12°C (53.6°F). Retrograde cerebral perfusion is then started via the superior vena cava.

Recent study results support the current standard of care in Central Europe for type A dissections. Outcomes with hypothermic circulatory arrest and antegrade cerebral perfusion in arrest times shorter than 30 minutes were similar. Antegrade cerebral perfusion with sufficient pressure is advised for arrest times longer than 30 minutes.[25]

The ascending aorta is inspected for the site and extent of the tear and the involvement of the transverse arch and for an assessment of intimal disruption that requires repair. Through a longitudinal approach, the ascending aorta is opened and transected just proximal to the innominate artery. If the transverse arch is free of reentry, the intima and adventitia are sutured together with fine 4-0 and 5-0 polypropylene suture. A gelatin- or collagen-woven Dacron graft is sutured to the reinforced proximal aortic arch in end-to-end fashion and reinforced from both inside and outside with 4-0 pledgeted sutures.

At the time of completion of the distal anastomosis, retrograde cerebral perfusion is stopped and cardiopulmonary bypass is restarted via the femoral artery. This evacuates all air and debris from the brachiocephalic vessels. The graft is clamped proximal to the origin of the innominate artery. Flow to the cerebral and systemic circulation is restored after clamping the graft proximal to the origin of the innominate artery.

Hypothermic circulatory arrest is a valuable tool in aortic dissection repair. Emptying the major vessels allows ingress of air, which causes complications related to air embolism, a major hazard associated with this procedure. Ensure that the patient's head is not elevated; rather, depress it and allow blood to gravitate into the head vessels, thus displacing the air (upward) to the periphery. This is essential.

The patient is rewarmed with restoration of anterograde flow through a side arm line inserted in the ascending aorta. The aortic valve is suspended with 4-0 polypropylene pledgeted sutures if it is normal and no evidence of aortic root dilatation is present. The intima and adventitia of the aorta superior to the coronaries are sutured together and reinforced from inside the graft. If the aortic valve or the root is dilatated, a composite valve graft is placed.

A button or modified Cabrol technique is used to reattach the coronaries. When aortic regurgitation is present, simple decompression of the false lumen may be all that is required to allow resuspension of the aortic leaflets and restoration of valvular competence. More often, however, the 2 layers of the dissected aortic wall are approximated, and resuspension of the commissures is accomplished with pledgeted sutures. Prosthetic aortic valve replacement also may be necessary in certain situations. After the procedure is completed and the patient is brought to sinus rhythm by defibrillation, the patient is weaned from cardiopulmonary bypass.

In patients with involvement of the transverse aortic arch, either the proximal arch or the total arch is replaced. If the intima is fragmented or shows evidence of rupture, then the whole arch is replaced.

Surgical management of acute type B aortic dissections is undertaken only in the presence of indications such as persistent pain, aneurysmal dilatation greater than 5 cm, end organ or limb ischemia, or evidence of retrograde dissection to the ascending aorta. The remaining patients are treated with intense medical therapy.[5]

The operation involves transection of the proximal descending aorta distal to the left subclavian artery. Similar to operation on the ascending aorta, the proximal and distal intima and adventitia of the transected aorta are reinforced in the same manner as that for the ascending aorta, with a 4-0 polypropylene suture. A gelatin- or collagen-woven Dacron graft is sewn directly to the reinforced acutely dissected proximal thoracic aorta, with the posterior row reinforced using interrupted polypropylene sutures. Blood is rechanneled into the true lumen of the distal aorta by cutting the descending thoracic graft and suturing it to the reinforced distal aorta.

Adjunct procedures are used to minimize complications. The entire thoracoabdominal aorta is opened if extensive involvement of the descending and abdominal aorta is present that requires replacement. The septum between the false and true lumen is excised, and the visceral vessels and renal arteries are reattached to the graft directly or via a Dacron graft.

In chronic dissections, the intercostal arteries (T9-T12) are reimplanted by side graft or a side hole. This is in contrast to acute dissections, in which the intercostals and lumbar arteries are ligated. Newer surgical techniques have been developed that use fibrin sealant or gelatin-resorcin-formaldehyde glue.

Glue replaces the use of pledgeted sutures to seal the false lumen of the aortic stumps after resection of the diseased aortic segment and before the implantation of the Dacron prosthesis. The glue hardens and reinforces the dissected aortic tissue. Other advantages include simplification of the operation, facilitation of the resuspension of the aortic valve, and, possibly, reduction in the frequency of late aortic root aneurysm formation.

Because of high operative mortality rates in people with renal or visceral artery compromise from dissection, endovascular techniques are under investigation. Several endovascular techniques are available.[15, 18, 26] One involves the formation of a site of reentry to allow blood to pass from the false lumen to the true lumen. This requires passing a wire past the intact intimal flap, passing a balloon-tipped catheter over the wire, and tearing a hole in the intimal flap by inflating the balloon.

Another technique involves percutaneous stenting to decrease the ischemic complications of aortic dissection. This is performed on arteries that have compromised flow from the dissection. Sutureless intraluminal prostheses placed during cardiopulmonary bypass are also being used. Another technique involves percutaneously placed intraluminal stent-grafts using a transfemoral catheter technique. This procedure results in the closure of the site of entry into the false lumen and decompresses and promotes thrombosis of the false lumen. It also alleviates obstruction of the branch vessels complicating a dissection.

Intramural hematomas and penetrating atherosclerotic ulcers of the aorta are conditions that result in aortic dissection or rupture. Both are more common in the descending aorta; medical therapy is the first-line treatment. When either affects the ascending aorta or the arch, the need for surgery is more likely. Intramural hematomas are hemorrhage into the medial layer of the aortic wall without an intimal tear. Because these hematomas have a natural history similar to aortic dissection and aneurysm, they are treated similarly.

Surgical therapy is initiated for patients with proximal hematomas; medical therapy is reserved for patients with distal hematomas. Medical therapy consists of optimizing blood pressure control, decreasing aortic pulse pressure, controlling risk factors for atherosclerosis, and maintaining close long-term follow-up care. Penetrating atherosclerotic ulcers penetrate the internal elastic lamina, causing hematoma formation within the media of the aortic wall. Almost all are in the descending aorta. Because the natural history of these ulcers is undefined, a definitive treatment strategy has not been formulated.

Consider surgery in patients with penetrating atherosclerotic ulcers who are hemodynamically unstable or who have evidence of pseudoaneurysm formation or transmural rupture. Other indications for surgery include recurrent pain, distal embolization, and progressive aneurysmal dilatation from the ulcer. If patients present without these complications, they are treated with antihypertensive medications and close monitoring.[27]

For endovascular therapy, the patient is prepared for general anesthesia and open procedure. The patient is then taken to the vascular suite and after the induction of general anesthesia, bilateral groin cutdowns are performed to gain access to the common femoral artery. Due to the large size of the sheath needed to introduce the stent, a synthetic graft may be sewn to the artery to gain access. Once groin access is obtained, the patient is heparinized and the stent is positioned and deployed using radiographic guidance.[24]

Outcome and Prognosis

Hospital-based mortality rates for aortic dissection are approximately 30%.

Patients with type A aortic dissection who undergo surgical treatment have a 30% mortality rate; patients who receive medical treatment have a mortality rate of 60%. Comorbidities and advanced aged can pose a contraindication to surgery in selected patients.

Future and Controversies

The aortic dissection mortality rate is still high despite advancements in diagnostic and therapeutic modalities.[1, 3] Ideally, researchers will devise a test that detects aortic dissection before severe complications develop, thus allowing early intervention and eventually reducing mortality rates.

The findings of the smooth muscle myosin heavy-chain assay are not elevated in persons with acute myocardial infarction or other nonaortic conditions of chest pain syndromes. The test's sensitivity and specificity are promising, and, in the future, a battery of tests will help determine a genetic predisposition to aortic dissection, including conditions such as Ehlers-Danlos syndrome and Marfan syndrome.

Aortic dissection. CT scan showing a flap (right side of image).

Aortic dissection. CT scan showing a flap (center of image).

Aortic dissection. CT scan showing a flap (center of image).

Aortic dissection. True lumen versus false lumen in an intimal flap.

Image A represents a Stanford A or a DeBakey type 1 dissection. Image B represents a Stanford A or DeBakey type II dissection. Image C represents a Stanford type B or a DeBakey type III dissection. Image D is classified in a manner similar to A but contains an additional entry tear in the descending thoracic aorta. Note that a primary arch dissection does not fit neatly into either classification.

Aortic dissection. Left subsegmental atelectasis and left plural effusion. Flap at lower right of image.

Aortic dissection. Significant left plural effusion.

Aortic dissection. Intimal flap and left plural effusion.

Aortic dissection.

Aortic dissection. CT scan showing a flap (right side of image).

Aortic dissection. True lumen versus false lumen in an intimal flap.

Aortic dissection. Left subsegmental atelectasis and left plural effusion. Flap at lower right of image.

Aortic dissection. CT scan showing a flap.

Aortic dissection. CT scan showing a flap.

Aortic dissection. Thrombus and a patent lumen.

Aortic dissection. Thrombus.

Aortic dissection. Mediastinal widening.

Aortic dissection. CT scan showing a flap.

Aortic dissection. Intimal flap and left plural effusion.

Image A represents a Stanford A or a DeBakey type 1 dissection. Image B represents a Stanford A or DeBakey type II dissection. Image C represents a Stanford type B or a DeBakey type III dissection. Image D is classified in a manner similar to A but contains an additional entry tear in the descending thoracic aorta. Note that a primary arch dissection does not fit neatly into either classification.